Mood disorders often have a seasonal onset or exacerbation, although the mechanism behind such seasonal triggers for psychopathology is still unknown. Many other disorders may also have such seasonal patterns of exacerbation. We hypothesize that abnormal responses to diminished levels of environmental light in winter may account for the regular winter timing of episodes of depression, seasonal changes in biology, and the benefit of light therapy in disorders like seasonal affective disorder, bipolar disorder, nonseasonal depression, eating disorders, and cognitive decline in aging, for example. Abnormal responses to environmental light levels may be mediated by abnormal retinal signaling. The aim of the present study is to determine if a specific pathway, the melanopsin pathway, originating in the retina and projecting to central brain areas, is involved in dysphoric mood, over eating, over sleeping, and fatigue in winter. A measure of the sensitivity of this neural pathway, the post-illumination pupil response (PIPR), will be tested for association with genetic variations in the melanopsin gene, seasonal changes in mood and behavior, and psychopathology (i.e., dysphoric mood, hypersomnia, hyperphagia, and fatigue). If diminished melanopsin photosensitivity is associated with seasonal decrements in mood, the PIPR may constitute a biomarker for this type of psychopathology, leading to a new way to classify psychopathology based on the pathway of origin, or the etiology. In the future, we may be able to use the PIPR test to identify those vulnerable to specific light-related exacerbation of psychopathology, and potentially to predict the best treatment for a given individual, reducing the trial-and-error of treatment, and reducing the time to recovery.